In man the renin angiotensin in a variety of clinical conditions including congestive heart failure, hepatic cirrhosis, hypotensive shock, and hypertension. Renin is released from the juxtaglomerular cells of the renal afferent arterioles under the control of: 1) sympathetic tone to the juxtaglomerular cells, 2) circulating humoral agents which act on thejuxtaglomerular cells, 3) a vascular receptor, thought to be the juxtaglomerular cells themselves, which responds to hemodynamic changes, and 4) a tubular receptor in the macula densa which is sensitive to the composition of the renal tubular fluid. Experimentally it is difficult to study the control of renin release by the three afferent arteriolar mechanisms in mammals because their stimulation generally alters the composition of the tubular fluid. This alteration can cause secondary changes in renin release mediated by the macula densa. Reptiles, however, have no macula densa yet have juxtaglomerular cells similar to mammals, making them an excellent model for studying the afferent arterior control mechanisms. The proposed study will examine the control of renin release in the turtle in response to: 1) renal nerve stimulation 2) adrenergic agonist and atagonist infusion, 3) catecholamine infusion, 4) angiotensin II infusion, and 5) acute renal blood pressure changes. Since the renin angiotensin system appears to be very similar in turtles and mammals, the results of studies in this model should be applicable to mammalian systems and will lead to a better understanding of the role of the nontubular mechanisms for controlling renin release.